Publication: Mutation, replicative infidelity of DNA and aneuploidy sequentially in the formation of malignant pleomorphic tumors
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Date
2007
Authors
Bignold, L.P.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Mutations are thought to be involved in
tumor formation because (i) tumor cells transmit their
abnormalities to their descendants; and (ii) many
carcinogens are mutagens. Aneuploidy is thought to be
involved in tumor formation because (i) it is a common
phenomenon, especially among malignant neoplasms;
(ii) certain particular types of tumors are associated with
specific karyotypic changes; and (iii) many immortal
tumor cell lines are hyperploid. In recent years, acquired
somatic cell replicative infidelity of DNA (“mutator
phenotype”) has been suggested as a mechanism of
tumor formation, because more somatic genomic events
occur in malignant tumor cells than could be caused by
repeated exogenous mutagenic insults. Previously,
theories of the genomic pathogenesis of tumors have
involved these mechanisms individually. Here it is
suggested that all three mechanisms may play roles in
the formation of certain tumor types. For example, a
sequence could occur such that first, a mutation affects
genomic elements for control of growth, and for
replicative fidelity of DNA, leading to “mutator
phenotype”. Second, when replicative infidelity of DNA
results in mutation of genomic elements for mitotic-andchromosomal
stability, aneuploidy develops. Third, an
asymmetric mitosis (in the course of the aneuploid stage)
could produce occasional cells in which the “bad copy”
is lost (or an extra “good copy” is gained) of the original genomic element which had supported replicative
fidelity of DNA. These resulting cells would regain
fidelity of replication of DNA, and hence could give rise
to populations which are relatively genomically stable,
hyperploid and immortal.
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